Tachy Therapy Was Again Turned on
HeartRhythm Case Rep. 2020 Sep; vi(ix): 622–626.
Ventricular tachycardia with therapy inappropriately withheld due to ventricular-based timing
Weixian Alex Tan
∗National Heart Centre Singapore, Singapore
Tien Siang Eric Lim
∗National Heart Centre Singapore, Singapore
Rachel Heo
†Abbott, Singapore
Chi Keong Ching
∗National Heart Centre Singapore, Singapore
Boon Yew Tan
∗National Center Middle Singapore, Singapore
Keywords: AV delay, Cardiac resynchronization therapy defibrillator, DDI, SyncAV, Timing cycles, Ventricular tachycardia
Introduction
Electrical optimization, which is manifested by the abridgement of the QRS duration, has been associated with improved cardiac resynchronization therapy (CRT) response.ane The introduction of a device-based algorithm (SyncAV) that automatically adjusts the atrioventricular delay (AVD) based on the intrinsic atrioventricular (AV) conduction has been shown to be superior in achieving QRS duration narrowing.ii Nosotros report a example in which our patient developed ventricular tachycardia (VT) with an unusual ane:one atrial tracking of the VT due to the SyncAV algorithm. As a result, antitachycardia therapy was inappropriately withheld.
Case report
A 75-year-old human being with an established history of ischemic cardiomyopathy underwent CRT-D (cardiac resynchronization therapy defibrillator) implantation in 2018 (St Jude Quadra Assura CD3367-40QC, Abbott, Singapore).
The device'due south pacing mode was DDDR with a base rate of xc beats per minute (bpm) and wheel length of 667 ms, which in Abbott's implantable cardioverter-defibrillator (ICD) relies on a modified atrial-based timing. The maximum sensing and tracking rates were programmed at 105 bpm. Tachycardia detection parameters were programmed equally follows: VT1 zone 160 bpm, VT2 zone 187 bpm, VF zone 250 bpm. The supraventricular tachycardia (SVT) discrimination timeout feature was programmed off.
He was admitted with VT storm and received multiple shocks. Intravenous amiodarone was initiated and this resulted in the prolongation of his AV nodal conduction to 300 ms at a base charge per unit of 90 bpm. The paced AVD was programmed at 350 ms to allow for appropriate paced AVD search with a 50 ms offset subsequently applied.
He developed VT at a rate of 163 bpm with a wheel length of 367 ms, as evidenced past the change in morphology seen on the telemetry strip (Effigy 1) during his stay and was establish unresponsive. Immediate external direct electric current cardioversion was successful in restoring sinus rhythm. Upon interrogation of his CRT-D, an episode of atrial pacing at a charge per unit of 163 bpm was seen with no antitachycardia therapy delivered from the device (Figure twoA and B). What was the mechanism for the apparent atrial "tracking" of his VT and why was therapy withheld? We further explain in our discussion below.
Telemetry strip showing APVP with prolonged AV delay (350 ms); subsequent change in rhythm and rate indicating ventricular tachycardia. Atrial paced issue circled in red indicates the probable inferred "bedroom of onset" of ventricular tachycardia as the atrium.
A: The earliest recording of tachycardia showed 1:1 atrial-to-ventricular complex association at 163 bpm. Green arrow: Ventricular tachycardia (VT) beat non sensed as it savage into post-atrial ventricular blanking. Blue pointer: Device delivered biventricular pacing, which fused with next VT beat. Majestic arrow: Native atrial shell, not tracked. Orange arrow: Functional noncapture of atrial paced issue. Ventriculoatrial (VA) interval is demonstrated in 2nd half of strip, with calculated VA interval hither: (AP-AP) – (AP-VS) = 367 – 55 = 312 ms. Similar to calculated VA interval 317 ms. B: The recording ended with this strip. When the VT slowed just sufficiently to fall beneath VT1 zone, following 5 beats of "VS" circled in cherry, the device declared "return to sinus," as indicated past the yellowish star. The device reverted to DDDR style as indicated, with a modified atrial-based timing; even so, the AP-AP interval highlighted in the blue box was unexpectedly prolonged at 758 ms. The crimson foursquare boxes of "VS" signal what the device interpreted every bit premature ventricular contractions, resulting in a conversion to ventricular-based timing.
Give-and-take
Effigy 2A illustrates the showtime electrogram recording by the device; unfortunately, the onset of VT was not captured. The electrogram shows VT occurring at a rate of 163 bpm and atrial pacing occurring at the aforementioned charge per unit with i:1 clan. Of note, the second VT beat (green arrow) was not sensed by the device every bit it fell within the post-atrial ventricular blanking (PAVB) period. PAVB in Abbott's devices are preset at either 44 ms or 52 ms, with 52 ms being the nominal setting, as information technology was in this example. Following this VT crush that was not sensed, the device delivered biventricular pacing (bluish arrow), which fuses with the adjacent VT beat. A native atrial shell then occurs (majestic arrow), which was not tracked, followed past a functional noncaptured atrial paced (AP) effect (orangish arrow).
At baseline, there was normal intrinsic AV nodal conduction. The SyncAV algorithm was switched on with a good abbreviation of the QRS duration. The SyncAV algorithm automatically extends the paced or sense AV delay (350 ms and 325 ms, respectively) for 3 beats afterward every 256 beats. During this time, the device measures the intrinsic AV interval before applying a programmable AVD showtime of 50 ms in our patient's case. This algorithm bicycle repeats every 256 beats, allowing for dynamic adjustment of the paced or sensed AV delay. If the sensed ventricular electrogram timing extends beyond 350 ms during atrial pacing or 325 mg during atrial sensing, which occurred in our patient'southward case owing to ongoing amiodarone therapy, SyncAV would maintain the AVD at these values. This is seen in Figure 1 where the AP–biventricular paced interval is 350 ms just earlier onset of VT.
During VT, Abbott'south devices employ an episodal pacing mode (DDI), which utilizes ventricular-based timing. This is to prevent forced ventricular pacing during the episode, should an atrial sensed event occur. With a base charge per unit of 90 bpm and cycle length of 667 ms, programmed paced AVD at 350 ms (as per the SyncAV algorithm with an AVD prolonged beyond 350 ms), the calculated ventriculoatrial (VA) interval is thus equal to 667 ms minus 350 ms, or 317 ms. This resulted in the apparent one:1 atrial "tracking" of the VT, where an AP event occurs afterwards every ventricular sense (VS) event with a VS-AP elapsing of 317 ms. The VT was "tracked" as each VS upshot occurred 59 ms after an AP event, just after the programmed PAVB of 52 ms.
Dual-chamber discrimination in Abbott's devices depends on the charge per unit branch algorithm. As there is one:1 AP-VS correlation during VT, it thus classified this episode under the Five=A charge per unit branch arm. Further discrimination then depends on morphology and/or chamber of onset. The bedchamber of onset was the atrium, which could exist inferred as the terminal AP spike on the telemetry strip in Figure 1 (the arrow circled in red). Even though the morphology of the VT did not friction match the sinus rhythm template, as both morphology and bedchamber of onset did not concord, therapy was thus withheld every bit the "IF ALL" criterion for VT was not met.
Information technology is important to maintain as close to 100% sensitivity for VT detection and therapy as possible, specially in our patient'due south case, given his recurrent VT episodes. As such, it would have been prudent to increase diagnostic sensitivity at some expense to specificity. In retrospect, the SVT high rate discrimination timeout feature could accept been turned on and the rate branch discriminator set to "IF ANY," which in this case would have delivered appropriate therapy for the VT episode. The balance between sensitivity and specificity of the device should be applied on a case-past-case basis, considering the patient'south history and likelihood of having episodes of VT vs SVT.
As a result of the higher up fortuitous events, VT continued, and the device withheld therapy. Subsequently, the VT rate slows for five beats to 158 bpm, bike length of 379 ms which was below the programmed VT1 zone of 160 bpm (Figure twoB). As a outcome, it triggered a "render to sinus" event, reverting to DDDR way with modified atrial-based timing. The diagnosis of VT then becomes painfully clear with more V > A. However, therapy was still withheld every bit the VT charge per unit now has fallen below the programmed VT1 zone.
In modified atrial-based timing during DDDR fashion, the cycle length between ii AP intervals is dictated by the atrial-atrial (A-A) interval, which is 667 ms at a base rate of 90 bpm, and non the VA interval. Interestingly, the AP-AP interval continues at a slower rate of 79 bpm, cycle length of 758 ms and not the expected 90 bpm (Effigy 2B). While the commencement VS episode did not initiate an AP event (DDDR, atrial-based timing), the second VS (Figure 2B, red square), with no preceding AP or atrial sensed event, would exist interpreted as a premature ventricular complex past the device, leading to an immediate conversion to a ventricular-based timing. Another AP would then exist delivered afterward a VA interval of 317 ms. The VT continues at this slower rate and the cycle repeats itself. The overall AP-AP bicycle length would thus exist equal to AP VS 66 ms + VT cycle length 379 ms + VA interval 317 ms, or 762 ms.
Later on this event, nosotros reprogrammed the device parameters every bit follows. Nosotros reduced the VT1 detection zone from a rate of 160 bpm to 141 bpm as the VT episode occurred at a rate of 158–163 bpm, which was just at the limits of the original VT1 zone. Furthermore, paced AVD was reduced from 350 to 130 ms, sensed AVD was reduced from 325 to 100 ms, and the SyncAV algorithm was turned off. This was attributable to the prolonged AV delay in our patient on amiodarone therapy and earlier witnessed deleterious effects of a long AV delay coupled with high programmed base rate and DDI mode during VT. We kept our patient on amiodarone therapy in view of his recurrent VT episodes, equally nosotros felt the likelihood of this recurrent event is depression given the abovementioned adjustments that were fabricated.
The role of an ICD is to care for malignant ventricular arrhythmias and prevention of sudden cardiac death is its fundamental office. However, with the combination of pacing function in the form of dual-bedchamber devices or biventricular devices and the advent of increasingly complex device programming algorithms, nosotros need to exist conscientious not to cause intradevice interaction that tin can potentially undermine the prime number purpose of the device.
Strohmer and colleagues3 take reported the association of atrial tachycardia and VT after dual-sleeping accommodation ICD implantation, as well as how frequent "physiological" AV pacing tin lead to proarrhythmic effects in ICD patients. For example, with dual-chamber pacing, an AP ≥48% together with VP >xl% was associated with increased likelihood of VT.3 Expanding on this ascertainment, one can imagine that, with the complexities of CRT-D programming, the potential for intradevice interaction is existent and hence physicians as well every bit manufacturers should be cognizant of these risks.
Glikson and colleagues4 reported in a prospective written report how a rate-smoothing algorithm resulted in a potential delayed or absent detection of ventricular tachyarrhythmias. When the algorithm is turned on, each R-R interval is used as a reference value and subsequent R-R interval is limited to a programmed percentage variation from the reference. The rate-smoothing algorithm was initially designed to reduce sudden changes in heart rate of patients with pacemakers and subsequently also showed some do good in reducing the initiation of ventricular arrhythmias through the prevention or shortening of the postextrasystolic intermission. Through a complex interplay between rate-smoothing parameters and VT detection, 6 out of ten cases of monomorphic VT had delayed or absent detection. It was highlighted that VT rates of <220 bpm, long AV delays, and high upper rates have a higher likelihood of affecting VT detection.4
Cooper and colleagues5 also reported a instance in which a biventricular ICD system failed to detect VT within its programmed VT detection zone, resulting in inappropriately withheld therapy. The identified cause was one time once more the rate-smoothing algorithm; however, unlike what Glikson and colleagues4 reported, in this case it was a short AV delay with slow VT (125 bpm) and small-scale maximum tracking charge per unit of 115 bpm that resulted in impaired VT detection. Owing to the charge per unit-smoothing-down algorithm, which directs the upper rate limit, AP events (using ventricular-based timing) and ventricular blanking periods can exist introduced into the VT detection zone and hence affect appropriate VT detection.5
Shalaby6 reported a case of VT with cycle length of 465 ms that was undersensed in a dual-chamber ICD owing to charge per unit-adaptive pacing. This was due to ventricular-based timing, which mandates that atrial pacing occurs at a fixed VA time, which coincidentally occurred close to the VT wheel length. Every bit a event, the subsequent VT crush fell within the PAVB period, resulting in undersensing of the VT and tachycardia therapy being inappropriately withheld.
Conclusion
The appearance of the SyncAV algorithm allows u.s. to achieve better abridgement of the QRS complex with CRT. The algorithm necessitates the programming of a long AVD to allow for an appropriate "search" of the intrinsic AVD. A nontracking DDI episodal mode during VT, which utilizes ventricular-based timing, together with a high programmed base rate and long paced AVD, results in a brusk VA interval and the apparent i:1 atrial "tracking" of the VT. There is thus a complex interplay between the programmed base rate, AVD, and the VT wheel length (Effigy three). As shown, a VT charge per unit of 163 bpm (in cherry-red) would result in 1:ane atrial "tracking" of the VT if a base rate of 90 bpm and a paced AVD of 350 ms is programmed. For any given VT cycle length, nosotros can thus reduce the likelihood of this miracle by judiciously avoiding the base of operations rates and AVD intervals, as illustrated in Figure 3. Other possible solutions would be to only switch off the SyncAV algorithm (at the cost of less QRS abridgement) and prefer the nominal short paced AVD, or to lengthen the PAVB (if this is a programmable characteristic).
Relationship between base rate, paced atrioventricular (AV) filibuster, and maximum ventricular tachycardia rate with one:one atrial tracking. The yellow star indicates the base rate and paced AV delay values that nosotros should avoid programming.
Our patient was fortunate to have had this episode occur during a monitored infirmary admission and received prompt treatment. The outcomes could take been significantly dissimilar and fatal had it occurred elsewhere. We are reminded through this case that intradevice interactions tin can occur with detrimental effects.
Footnotes
This enquiry did not receive whatever specific grant from funding agencies in the public, commercial, or not-for-profit sectors. The authors have no conflicts of interest to disclose.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7498506/
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